Gene–gene interactions of the Wnt/β-catenin signaling pathway in knee osteoarthritis

Fernández‐Torres, Javier; Zamudio-Cuevas, Yessica; López‐Reyes, Alberto; Garrido-Rodríguez, Daniela; Martínez-Flores, Karina; Lozada, Carlos; Muñoz‐Valle, José Francisco; Edith, Oregon-Romero; Martínez‐Nava, Gabriela Angélica

doi:10.1007/s11033-018-4260-2

Cited by 19 publications

(10 citation statements)

References 39 publications

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“…Consistent with the literature, this research found that silence of HOTAIR inhibited inflammation response and oxidative stress in oxidized low-density lipoprotein-treated human macrophages by climbing miR-330-5p [25]. The Wnt/β-catenin pathway occupies a vital part in the regulation, proliferation, differentiation and cellular death processes [13]. This also accorded with the earlier observations, which made it clear that the Wnt/β-catenin pathway could be activated in IL-1β-induced chondrocytes [22].…”

Section: Discussionsupporting

confidence: 88%

“…Wnt/β-catenin signaling takes a central part in liver tumor-initiating cells selfrenewal, and its activation is under accurate regulation [12]. As reported, the Wnt pathway is an necessary mechanism in the cartilage development and bone remodeling, and Wnt/β-catenin pathway is involved in knee OA pathogenesis [13]. The Wnt/β-catenin signaling pathway in an activated condition has been conveyed to be a cause for escalated β-catenin levels in articular cartilage and could further result in cartilage changes in OA at the early stage [14].…”

Section: Introductionmentioning

confidence: 92%

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RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

Tian

et al. 2019

Cell Cycle

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Osteoarthritis (OA) is a degenerative injury of the articular cartilage and reactive hyperplasia of the articular rim and subchondral bone. Due to its poor prognosis, this study is to research the influences of lncRNA HOTAIR on synovial inflammation and synoviocyte apoptosis and proliferation in OA rats by regulating the Wnt/β-catenin pathway. Rat OA model was constructed by means of cruciate ligament resection, and the successfully modeled rats were injected with sh-HOTAIR, or Wnt/β-catenin pathway activator (LiCl), and synoviocytes were transfected with sh-HOTAIR or LiCl for investigation of the influences of HOTAIR and Wnt/β-catenin pathway on synoviocytes proliferation and apoptosis. ELISA and RT-qPCR were used to detect the levels of IL-1β, IL-6 and TNF-α in serum, synovial tissue and synoviocytes in rats, respectively. The protein levels of bax, bcl-2, wnt1 and β-catenin in synovial tissue and synoviocytes were tested by Western blot analysis. Highly expressed HOTAIR existed in synovial tissue and synoviocytes of rats. There were declining arthritis index, inflammation, synoviocytes proliferation, cycle progression and promoted synoviocytes apoptosis by silencing HOTAIR and inhibited Wnt/β-catenin pathway. Down-regulation of HOTAIR could reverse the effect of LiCl on progression of OA rats. There was strained activation of Wnt/β-catenin pathway via declining HOTAIR. This study suggests that silencing lncRNA HOTAIR and inhibited Wnt/β-catenin pathway decline synovial inflammation and synoviocyte proliferation and promote apoptosis in OA rats.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 92%

RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

Tian

et al. 2019

Cell Cycle

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“…Numerous signaling pathways are involved in the process of OA, including bone morphogenetic proteins (8), Indian hedgehog (9), hypoxia-induced and Wnt signaling pathways (10,11). As an important component of the Wnt signaling pathway, β-catenin is activated by Wnt family proteins and participates in the pathological process of KOA (12). Previous studies have also demonstrated that the Wnt signaling pathway is involved in the homeostasis and degradation of the cartilage matrix by regulating the expression of anabolic or catabolic genes, such as increased expression of MMP-2, MMP-3, MMP-9, MMP-13, AdAMTS4 and AdAMTS5, which promote the degradation of the extracellular matrix and trigger KOA (13).…”

Section: Introductionmentioning

confidence: 99%

The GSK‑3β/β‑catenin signaling pathway is involved in HMGB1‑induced chondrocyte apoptosis and cartilage matrix degradation

et al. 2020

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Knee osteoarthritis (KOA) is a common joint disease with a high incidence rate among middle-aged and elderly individuals. However, the precise underlying pathological mechanisms and effective treatment of this disease remain to be determined. To explore the effect of high mobility group box 1 (HMGB1) on chondrocyte apoptosis and catabolism, the ATdc5 cell line was cultured as an in vitro model for cartilage research. cultured cells were treated with recombinant HMGB1 at different concentrations. Hoechst staining and flow cytometry demonstrated that HMGB1 administration significantly induced apoptosis of ATdc5 cells, which was the same as the effect of interleukin-1β treatment. HMGB1 also induced cartilage matrix degradation, as shown by Alcian blue staining. Moreover, HMGB1 markedly upregulated the expression levels of matrix metallopeptidases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (AdAMTS), while genetic silencing of HMGB1 significantly suppressed their expressions. The glycogen synthase kinase (GSK)-3β/β-catenin pathway was activated upon HMGB1 treatment. Pharmacological inhibitors or HMGB1 knockdown inactivated the GSK-3β/β-catenin pathway, inhibited the expression levels of downstream genes, including MMPs and AdAMTS, and attenuated the apoptosis of ATdc5 cells. Furthermore, the data demonstrated that HMGB1 promoted chondrocyte dysfunction via the regulation of estrogen sulfotransferase and Runt-related transcription factor 2. Thus, the findings of the present study demonstrated that HMGB1 induces chondrocyte cell apoptosis via activation of GSK-3β/β-catenin and the subsequent expression of multiple targeted genes.

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“…In recent years, a great number of miRs, such as miR‐34a, miR‐27b, miR‐146a, and miR‐140, have been reported to be connected with OA pathogenesis 9 . Meanwhile, a study has suggestedthat gene‐gene interactions in the Wnt/β‐catenin signaling pathway plays a part in the etiology of knee OA 20 . Therefore, this study was to investigate how miR‐106 mediated Wnt3a/β‐catenin signaling pathway in the regulation of proliferation, differentiation, and apoptosis of chondrocytes in OA mice.…”

Section: Discussionmentioning

confidence: 99%

Downregulated microRNA‐106 inhibits apoptosis and promotes proliferation and differentiation of chondrocytes in osteoarthritis through restraining the activation of Wnt/β‐catenin pathway

Tao

Zhou

2020

The Kaohsiung J of Med Scie

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Osteoarthritis (OA) is a degenerative disease with poor prognosis. Recent studies demonstrated the change of several microRNAs (miRNAs) in OA and their possibility to be regarded as diagnostic markers for OA. This study was to investigate how miR‐106 mediated the Wnt3a/β‐catenin signaling pathway in the regulation of proliferation, differentiation, and apoptosis of chondrocytes in OA mice. A mouse OA model was established by using a modified Hulth modeling method. The mice were injected with miR‐106 Agomir or Antagomir to elucidate the role of miR‐106 in pathological structure, cell apoptosis, and inflammation reaction in cartilage tissues of OA mice. The chondrocytes were introduced with miR‐106 Inhibitor or Mimic to probe into the role of miR‐106 in proliferation, differentiation, and apoptosis of chondrocytes. RT‐qPCR and Western blot analysis tested miR‐106, Wnt3a, and β‐catenin expression. Elevated miR‐106 and activated Wnt3a/β‐catenin pathway were presented in cartilage tissues of OA mice. Inhibited miR‐106 declined Wnt3a and β‐catenin expression in cartilage tissues of mice of OA. Declined miR‐106 alleviated pathological changes, inhibited cell apoptosis and inflammation in cartilage tissues, promoted proliferation and differentiation, and suppressed apoptosis of chondrocytes in OA mice. Inactivating the Wnt3a/β‐catenin signaling pathway reversed the up‐regulated miR‐106‐induced suppression of chondrocyte proliferation and deterioration of bone and joint injury. This work makes it clear that downregulated miR‐106 suppresses apoptosis, and promotes the proliferation and differentiation of OA chondrocytes via inactivation of the Wnt3a/β‐catenin pathway, offering a novel treatment approach for human OA.

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Gene–gene interactions of the Wnt/β-catenin signaling pathway in knee osteoarthritis

Cited by 19 publications

References 39 publications

RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

RETRACTED ARTICLE: Silencing lncRNA HOTAIR declines synovial inflammation and synoviocyte proliferation and promotes synoviocyte apoptosis in osteoarthritis rats by inhibiting Wnt/β-catenin signaling pathway

The GSK‑3β/β‑catenin signaling pathway is involved in HMGB1‑induced chondrocyte apoptosis and cartilage matrix degradation

Downregulated microRNA‐106 inhibits apoptosis and promotes proliferation and differentiation of chondrocytes in osteoarthritis through restraining the activation of Wnt/β‐catenin pathway

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